The overall objective of the Computational Genomics Core is to use the state-of-the-art mathematical and computational approaches needed to better understand the complex systems biology presented by injury and critical illness. In addition, built on our developments and experiences in computational biology in the Inflammation and the Host Response to Injury Glue Grant, the Core is also designed to tackle several current computational challenges in translational research of injury. The major functions of the core are: (1) Investigate via computational analyses the genomic mechanism of the adaptive and maladaptive physiological responses to thermo injury in studies of the Research Projects, (la) Develop computational tools for using new exon-junction arrays in detection of gene expression and alternative splicing in animal models (mouse and Rhesus monkeys);(1b) Analyze the genomic effect of activation and/or inhibition of genes important to insulin resistance and mitochondrial dysfunction in animal models;and (1c) Compare cross species the genomic changes between animal models and burn patients, and between LPS and burns. Our goal in this program is using computational analysis to comprehensively identify and catalog the similarities and differences between these inflammatory sources and between patients and model systems. (2) Integrate the genomic, protein activity and metabolic data of the Center for rational target identification of gene candidates for intervention. (2a) Establish a disease specific knowledge-base of molecular derangements in skeletal muscle following thermal injury by integrating findings of the Center Projects with the information systematically harvested from the literature as well as the human transcriptome data of burn patients;(2b) Conduct computational analysis to identify key gene regulators as candidates for intervention studies. (3) Establish web-based portal of the data and knowledgebase as central community resource. Data warehousing and providing web-accessible sharing of the data and results with the research community. Importantly, the successful accomplishments will be achieved by the multidisciplinary group effort of close collaborations between bioinformaticians and statisticians, and the other investigators in the Center.
The Computational Genomics Core will develop and apply mathematical and computational methods to analyze, integrate, and share the large amount of research data and findings from the Center as well as the research community in order to understand the molecular mechanism of burn injury and subsequently help identify new targets for intervention. The ultimate goal is to search for better treatments of thermo injury.
|Zhao, Gaofeng; Yu, Yong-Ming; Kaneki, Masao et al. (2015) Simvastatin reduces burn injury-induced splenic apoptosis via downregulation of the TNF-?/NF-?B pathway. Ann Surg 261:1006-12|
|Watada, Susumu; Yu, Yong-Ming; Fischman, Alan J et al. (2014) Evaluation of intragastric vs intraperitoneal glucose tolerance tests in the evaluation of insulin resistance in a rodent model of burn injury and glucagon-like polypeptide-1 treatment. J Burn Care Res 35:e66-72|
|Zhao, Gaofeng; Yu, Yong-Ming; Shoup, Timothy M et al. (2014) Membrane potential-dependent uptake of 18F-triphenylphosphonium--a new voltage sensor as an imaging agent for detecting burn-induced apoptosis. J Surg Res 188:473-9|
|Carter, Edward A; Paul, Kasie; Bonab, Ali A et al. (2014) Effect of exercise on burn-induced changes in tissue-specific glucose metabolism. J Burn Care Res 35:470-3|
|Lee, Sangseok; Yang, Hong-Seuk; Sasakawa, Tomoki et al. (2014) Immobilization with atrophy induces de novo expression of neuronal nicotinic *7 acetylcholine receptors in muscle contributing to neurotransmission. Anesthesiology 120:76-85|
|Fu, Glenn K; Xu, Weihong; Wilhelmy, Julie et al. (2014) Molecular indexing enables quantitative targeted RNA sequencing and reveals poor efficiencies in standard library preparations. Proc Natl Acad Sci U S A 111:1891-6|
|Khan, Mohammed A S; Sahani, Nita; Neville, Kevin A et al. (2014) Nonsurgically induced disuse muscle atrophy and neuromuscular dysfunction upregulates alpha7 acetylcholine receptors. Can J Physiol Pharmacol 92:1-8|
|Ueda, Masashi; Iwasaki, Hajime; Wang, Shuxing et al. (2014) Cannabinoid receptor type 1 antagonist, AM251, attenuates mechanical allodynia and thermal hyperalgesia after burn injury. Anesthesiology 121:1311-9|
|Ibrahim, Amir; Fagan, Shawn; Keaney, Tim et al. (2014) A simple cost-saving measure: 2.5% mafenide acetate solution. J Burn Care Res 35:349-53|
|Shank, Erik S; Martyn, Jeevendra A; Donelan, Mathias B et al. (2014) Ultrasound-Guided Regional Anesthesia for Pediatric Burn Reconstructive Surgery: A Prospective Study. J Burn Care Res :|
Showing the most recent 10 out of 77 publications